Regulation of HP1–chromatin binding by histone H3 methylation and phosphorylation
By W. Fischle, Boo Shan Tseng, Holger L. Dormann, Beatrix Ueberheide, Benjamin A. Garcia, J. Shabanowitz, Donald F. Hunt, H. Funabiki, C. D. Allis. Nature, 2005
1,055 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/a2904df8d65e4cb3c07f6895519bf0fd6a527f4b
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cell Biology
In Molecular Biology
- Ryuji Hamamoto
- Yusuke Nakamura
- G. Toyokawa
- D. Reinberg
- Hyun-soo Cho
- S. Hayami
- Matthias Mann
- N. Dohmae
Citations in the corpus
- Repetitive centromeric satellite RNA is essential for kinetochore formation and cell division (2014, background): “Most HP1 protein typically dissociates from chromosomes during mitosis in an H3 serine 10 phosphorylated manner (Fischle et al., 2005; Hirota et al., 2005).”
- Ki-67: more than a proliferation marker (2018, background): “Additionally, the existing data provide an apparantly paradoxical scenario: although Ki-67 is required for the 3Dorganization of H3K9me3 foci, all three HP1 isoforms maintained their cellular localization in Ki-67-depleted cells (Sobecki et al. 2016).”
- Shared and separate functions of polo-like kinases and aurora kinases in cancer (2010, background): “Aurora kinase B phosphorylates histone H3 in G2 and promotes the dissociation of heterochromatin protein 1α (HP1α; also known as CBX5), HP1β (also known as CBX1) and HP1γ (also known as CBX3) from chromati”
- The Language of Histone Crosstalk (2010, background): “For example, heterochromatin protein 1 (HP1), which binds methylated H3K9, cannot do so when the adjacent serine 10 (H3S10) is phosphorylated during mitosis or during gene activation (Fischle et al., 2005; Mateescu et al., 2008).”
- Chromatin Structure and the Inheritance of Epigenetic Information (2010, background): “Histone PTMs on different residues have also been reported to be exclusive in some cases, such as H3S10 phosphorylation and H3K9me3 (Ref”
- Child health, developmental plasticity, and epigenetic programming. (2011, background): “Another level of cross talk involves removal or recruitment of a protein complex by an adjacent modification, as is the case for phosphorylation of serine 10 on histone H3, which is necessary to disrupt the binding of the heterochromatin protein 1 (HP1) to H3K9me3 (83).”
- BAC TransgeneOmics (2008, background): “LAP-tagged HP1β was readily detectable at its proper location in the nucleus and showed the expected dynamics through the cell cycl”
- Non-commercial Research and Educational Use including without Limitation Use in Instruction at Your Institution, Sending It to Specific Colleagues That You Know, and Providing a Copy to Your Institution's Administrator. All Other Uses, Reproduction and Distribution, including without Limitation Comm (2005, neutral): “(1) in which all the dipole–dipole couplings and chemical shielding parameters are varied.”
- Enhanced expression of EHMT2 is involved in the proliferation of cancer cells through negative regulation of SIAH1. (2011, methodology): “Many types of tumors and corresponding nonneoplastic tissues were prepared in 8-μm sections, as described previously [4].”
- How chromatin-binding modules interpret histone modifications: lessons from professional pocket pickers (2007, background): “For example, phosphate-mediated 'phospho-methyl switching' has been proposed and shown experimentally to control the release of more stably bound chromatin effectors, such as HP1 bound to H3K9me during mitosis and probably additional effectors bound during other cell-cycle and developmentally regula”
- Histone Modifications and Cancer. (2016, background): “H3 serine 10 phosphorylation adjacent to the trimethylated H3 (H3K9me3S10ph) by Aurora B causes dissociation of HP1 from heterochromatin during M phase and allows for mitotic progression (Fischle et al. 2005; Hirota et al. 2005).”
- Quantitative interaction proteomics and genome-wide profiling of epigenetic histone marks and their readers. (2010, background): “Phosphorylation of histone H3S10 results in the release of HP1 from chromatin during mitosis even though levels of H3K9me3 remain unchanged (Fischle et al., 2005).”
- Reading protein modifications with interaction domains (2006, background): “During mitosis, the Aurora-B kinase phosphorylates Ser10 of histone H3 (a known 14-3-3 protein -binding site), which displaces HP1 even though Lys9 remains in a trimethylated stat”
- Regulation of nucleosome dynamics by histone modifications (2013, positive): “Binding of HP1 chromo-domains to peptides harboring H3K9me3 is severely impaired by H3S10 phosphorylation (H3S10p), and the co-occurrence of H3K9me3 and H3S10p coincides with the release of HP1 from mitotic chromatin 60,61 .”
- Epigenetics: A Landscape Takes Shape (2007, background): “In addition, effector-repulsive functions have been demonstrated in which histone modifications abrogate the binding of particular effectors (Fischle et al., 2005; T.H. Bestor, personal communication).”